Investigation of JAM-A (rs790056) and LFA-1 (rs8058823) gene variants in Turkish colorectal cancer patients

Çaykara, Burcu; Alsaadoni, Hani; Pençe, Halime Hanım; Pençe, Sadrettin; Yilmaz-Aydogan, Hülya; Taştekin, Didem

doi:10.5152/tjg.2019.19141

Cited by 3 publications

(4 citation statements)

References 25 publications

(27 reference statements)

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“…Therefore, we aimed to determine the distributions of JAM-A rs790056 and LFA-1 rs2230433 variations in patients with leiomyoma, as well as their individual and combined effects. So far, studies investigating JAM-A and LFA-1 have been related to melanoma, coronary artery diseases (22), atherosclerosis (23), breast cancer ( 16), cerebral ischemiareperfusion injury (24), kidney cancer (25)and colorectal cancers (26). To our knowledge, JAM-A and LFA-1 gene variations in leiomyoma have been investigated for the first time in our study.…”

Section: Discussionmentioning

confidence: 80%

Analysis of JAM-A T>C (rs790056) and LFA-1 2120 G>C (rs2230433) gene variations in uterine leiomyoma

Karuserci

Tanoğlu

Pençe

et al. 2021

Anatolian Current Medical Journal

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Aim:We aimed to investigate the effect of junctional adhesion molecule-A (JAM-A) and lymphocyte function-associated antigen 1 (LFA-1) gene variants on the development of leiomyoma in Turkish women. Material and Method: Retrospectively, leiomyoma tissues from 102 patients who were operated due to leiomyoma between May 2018 and April 2019 and healthy myometrium tissues from 70 control group patients without leiomyoma who underwent hysterectomy due to other reasons were included in the study. JAM-A rs790056 (T>C) and LFA-1 rs2230433 (G>C) gene variants in all tissues were examined by the quantitative real-time polymerase chain reaction (qRT-PCR) technique. Statistical analyses were performed using SPSS 16 software package. Results: The frequency of JAM-A rs790056 CC genotype and C allele was significantly higher in the leiomyoma group compared to the control group (p=0.01, p=0.02), as well as the LFA-1 rs2230433 GG genotype which was also higher compared to the control group (p=0.01). Conclusion: JAM-A rs790056 was found to be more effective than LFA-1 rs2230433 in determining the risk of uterine leiomyoma. According to the results, it has been determined that variations in JAM-A and LFA-1 genes may cause predisposition to uterine leiomyoma in Turkish women.

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Section: Discussionmentioning

confidence: 80%

Analysis of JAM-A T>C (rs790056) and LFA-1 2120 G>C (rs2230433) gene variations in uterine leiomyoma

Karuserci

Tanoğlu

Pençe

et al. 2021

Anatolian Current Medical Journal

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“…Colorectal cancer is one of the deadliest carcinoma types worldwide. Recent research of the involvement of F11R/JAM-A and LFA-1 genetic variants in colorectal cancer development and metastasis was the first investigation of these gene variations in patients [ 110 ]. The authors revealed that the F11R/JAM-A rs790056 variation could influence the development of colorectal carcinoma (CC genotype has a threefold increased risk of colorectal cancer occurrence) and suggested that this variation could be evaluated as a potential predictive biomarker of this cancer type.…”

Section: F11r/jam-a Expression In Cancermentioning

confidence: 99%

“…The authors revealed that the F11R/JAM-A rs790056 variation could influence the development of colorectal carcinoma (CC genotype has a threefold increased risk of colorectal cancer occurrence) and suggested that this variation could be evaluated as a potential predictive biomarker of this cancer type. Unfortunately, they did not define the relationship between genotypes and F11R/JAM-A expression (protein expression and soluble F11R/JAM-A levels or mRNA were not measured) [ 110 ].…”

Section: F11r/jam-a Expression In Cancermentioning

confidence: 99%

The F11 Receptor (F11R)/Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A) in cancer progression

2021

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The F11 Receptor (F11R), also called Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A), is a transmembrane glycoprotein of the immunoglobulin superfamily, which is mainly located in epithelial and endothelial cell tight junctions and also expressed on circulating platelets and leukocytes. It participates in the regulation of various biological processes, as diverse as paracellular permeability, tight junction formation and maintenance, leukocyte transendothelial migration, epithelial-to-mesenchymal transition, angiogenesis, reovirus binding, and platelet activation. Dysregulation of F11R/JAM-A may result in pathological consequences and disorders in normal cell function. A growing body of evidence points to its role in carcinogenesis and invasiveness, but its tissue-specific pro- or anti-tumorigenic role remains a debated issue. The following review focuses on the F11R/JAM-A tissue-dependent manner in tumorigenesis and metastasis and also discusses the correlation between poor patient clinical outcomes and its aberrant expression. In the future, it will be required to clarify the signaling pathways that are activated or suppressed via the F11R/JAM-A protein in various cancer types to understand its multiple roles in cancer progression and further use it as a novel direct target for cancer treatment.

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“…Moreover, it regulates many cellular processes, including angiogenesis (Naik et al, 2008), cell migration (Azari et al, 2010;Wang and Liu, 2022) and adhesion (Mandell et al, 2005), leukocyte transendothelial migration (Corada et al, 2005;Khandoga et al, 2005), intercellular permeability (Laukoetter et al, 2007), epithelial-tomesenchymal transition (EMT) (Communal et al, 2020) and platelet activation (Babinska et al, 2002). In the literature, JAM-A is described as a protein involved in the pathogenesis of neurological disorders (Padden et al, 2007), cardiovascular diseases (Babinska et al, 2019;Koenen and Weber, 2022;Rath et al, 2022;Wang and Chen, 2022), rheumatoid arthritis (Fang et al, 2016), inflammatory bowel disease (Vetrano and Danese, 2009), and many types of neoplastic diseases including breast (McSherry et al, 2009;Murakami et al, 2011;Vellanki et al, 2019;Bednarek et al, 2020;Vences-Catalan et al, 2021;Smith et al, 2022), lung (Magara et al, 2017;Zhao et al, 2017), nasopharyngeal (Jiang et al, 2019;Dai et al, 2021), head and neck (Kurose et al, 2016;Kakiuchi et al, 2021), testicular (Tarulli et al, 2013), thyroid (Orlandella et al, 2019), colorectal (Caykara et al, 2019;Lampis et al, 2021), gastric (Huang et al, 2014), endometrial (Koshiba et al, 2009), cervical (Akimo...…”

Section: Introductionmentioning

confidence: 99%

Junctional adhesion molecule-A (JAM-A) in gynecological cancers: Current state of knowledge

Czubak-Prowizor¹,

Świątkowska²

2023

Biocell

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Junctional adhesion molecule-A (JAM-A), also known as the F11 receptor (F11R), is one of the tight junction components. JAM-A is a transmembrane glycoprotein that regulates many cellular processes, i.e., angiogenesis, leukocyte transendothelial migration, intercellular permeability, epithelial-to-mesenchymal transition, and platelet activation. Of note, it is involved in the pathogenesis of various cancer types, including gynecological cancers. Only a few studies are available about this cancer type. Observed aberrant JAM-A expression in gynecological cancers correlates with poor patient prognosis. To the best of our knowledge, conflicting JAM-A roles in various cancer types suggest that its involvement is complex and tumor-type specific. The underlying molecular mechanisms and pathways responsible for JAM-A functions were not fully elucidated and need to be identified. Finding appropriate novel molecular cancer biomarkers may reduce observed very high mortality rates and could contribute to personalized treatment development. The main aim of the present viewpoint article is to report the current knowledge about JAM-A participation in gynecological malignancies.

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Investigation of JAM-A (rs790056) and LFA-1 (rs8058823) gene variants in Turkish colorectal cancer patients

Cited by 3 publications

References 25 publications

Analysis of JAM-A T>C (rs790056) and LFA-1 2120 G>C (rs2230433) gene variations in uterine leiomyoma

Analysis of JAM-A T>C (rs790056) and LFA-1 2120 G>C (rs2230433) gene variations in uterine leiomyoma

The F11 Receptor (F11R)/Junctional Adhesion Molecule-A (JAM-A) (F11R/JAM-A) in cancer progression

Junctional adhesion molecule-A (JAM-A) in gynecological cancers: Current state of knowledge

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